Direct and indirect roles of viral suppressors of RNA silencing in pathogenesis.

Center for Plant Cell Biology, Department of Plant Pathology and Microbiology, University of California, Riverside, California 92521, USA.
Annual Review of Phytopathology (Impact Factor: 11). 10/2008; 46:303-26. DOI: 10.1146/annurev.phyto.46.081407.104746
Source: PubMed

ABSTRACT Plant and animal viruses overcome host antiviral silencing by encoding diverse viral suppressors of RNA silencing (VSRs). Prior to the identification and characterization of their silencing suppression activities mostly in transgene silencing assays, plant VSRs were known to enhance virus accumulation in the inoculated protoplasts, promote cell-to-cell virus movement in the inoculated leaves, facilitate the phloem-dependent long-distance virus spread, and/or intensify disease symptoms in systemically infected tissues. Here we discuss how the various silencing suppression activities of VSRs may facilitate these distinct steps during plant infection and why VSRs may not play a direct role in eliciting disease symptoms by general impairments of host endogenous small RNA pathways. We also highlight many of the key questions still to be addressed on the role of viral suppression of antiviral silencing in plant infection.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Rice grassy stunt virus (RGSV) is a member of the genus Tenuivirus, which includes rice stripe virus (RSV), as the type species. A viral suppressor of RNA silencing (VSR) of RGSV has not been identified, whereas the p3 protein of RSV (RSVp3) encoded by the viral-sense (v) strand of RNA 3 has been reported to act as a VSR. In this study, we examined the VSR function of the p5 protein of RGSV (RGSVp5), encoded by vRNA 5. Expecting it to correspond to the vRNA 3 of RSV, we compared the VSR function of RGSVp5 with that of RSVp3. In an Agrobacterium-mediated transient expression assay using a transgenic line of Nicotiana benthamiana that expressed green fluorescent protein and the wild type, RGSVp5 suppressed sense transgene-mediated post-transcriptional gene silencing (S-PTGS), inverted-repeat (IR) transgene-induced PTGS (IR-PTGS), and the systemic spread of GFP silencing, as in the case with RSVp3. By contrast, a gel mobility shift assay revealed that RGSVp5 did not have any distinct binding activity with 21-, 22-, or 24-nucleotide small interfering RNA (siRNA) duplexes, whereas RSVp3 binds to all three sizes of siRNA duplexes. Furthermore, the transiently expressed p5 protein fused with GFP was dispersed mainly in the cytoplasm, whereas the GFP-fused p3 protein of RSV was localized both in the nucleus and in the cytoplasm. Our results suggest that RGSVp5 functions as a VSR but that the suppression mechanism of RNA silencing and the subcellular localization of RGSVp5 differ from those of the analogous VSR, RSVp3, even in the same genus. Copyright © 2015. Published by Elsevier B.V.
    Virus Research 03/2015; 203. DOI:10.1016/j.virusres.2015.03.010 · 2.83 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Higher plants use RNA silencing to defend against viral infections. As a counter defense, plant viruses have evolved proteins that suppress RNA silencing. Mealybug wilt of pineapple (MWP), an important disease of pineapple, has been associated with at least three distinct viruses, Pineapple mealybug wilt associated virus -1, -2, and -3 (PMWaV-1, -2, and -3). Selected open reading frames (ORFs) of PMWaV-1 and PMWaV-2 were screened for their local and systemic suppressor activities in Agrobacterium-mediated transient assays using green fluorescent protein (GFP) in Nicotiana benthamiana. Results indicate that PMWaV-2 utilizes a multiple-component RNA silencing suppression mechanism. Two proteins, p20 and CP, target both local and systemic silencing in N. benthamiana, while the p22 and CPd proteins target only systemic silencing. In the related virus PMWaV-1, we found that only one of the encoded proteins, p61, had only systemic suppressor activity. Of all the proteins tested from both viruses, only the PMWaV-2 p20 protein suppressed local silencing induced by double-stranded RNA (dsRNA), but only when low levels of inducing dsRNA were used. None of the proteins analyzed could interfere with the short distance spread of silencing. We examined the mechanism of systemic suppression activity by investigating the effect of PMWaV-2-encoded p20 and CP proteins on secondary siRNAs. Our results suggest that the PMWaV-2 p20 and CP proteins block the systemic silencing signal by repressing production of secondary siRNAs. We also demonstrate that the PMWaV-2 p20 and p22 proteins enhanced the pathogenicity of Potato virus X in N. benthamiana.
    Viruses 03/2015; 7(3):969-995. DOI:10.3390/v7030969 · 3.28 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: On October 28th 1943 Winston Churchill said "we shape our buildings, and afterward our buildings shape us" (Humes, 1994). Churchill was pondering how and when to rebuild the British House of Commons, which had been destroyed by enemy bombs on May 10th 1941. The old House had been small and insufficient to hold all its members, but was restored to its original form in 1950 in order to recapture the "convenience and dignity" that the building had shaped into its parliamentary members. The circular loop whereby buildings or dwellings are shaped and go on to shape those that reside in them is also true of pathogens and their hosts. As obligate parasites, pathogens need to alter their cellular host environments to ensure survival. Typically pathogens modify cellular transcription profiles and in doing so, the pathogen in turn is affected, thereby closing the loop. As key orchestrators of gene expression, non-coding RNAs provide a vast and extremely precise set of tools for pathogens to target in order to shape the cellular environment. This review will focus on host non-coding RNAs that are manipulated by the infamous intracellular pathogen, the human immunodeficiency virus (HIV). We will briefly describe both short and long host non-coding RNAs and discuss how HIV gains control of these factors to ensure widespread dissemination throughout the host as well as the establishment of lifelong, chronic infection.
    Frontiers in Genetics 03/2015; 6:108. DOI:10.3389/fgene.2015.00108